Twitter icon
Facebook icon
Google icon
LinkedIn icon

Tension Pneumothorax

David Page MS, NREMT-P

Tension Pneumothorax

EMS Reference editor's note: This article is co-authored by Samuel Chu, BSE, NREMT-P, L. Michael Bowen, NREMT-P, and Katie Lyman, PhD, ATC, NREMT, CKTI.

 

Introduction

The thoracic cavity houses the heart, great vessels, diaphragm, lungs, and other vital organs. Because of this, any injury to the thoracic cavity can be rapidly lethal. Even small changes in the mechanics of oxygen exchange and circulation can have dire consequences for the patient.

Tension pneumothorax is a rapidly lethal condition in which a damaged lung, bronchus, or bronchiole allows air to enter the chest cavity. As more air enters the pleural space, a buildup of pressure causes collapse of the affected lung, shifting of the mediastinum and compression of the structures in the chest, impairing ventilation and perfusion.1 The structures affected are the lungs, the heart and great vessels, including the vena cava. The resulting increase in intrathoracic pressure reduces venous return to the heart, decreasing cardiac output, and poor ventilation rapidly creates a deadly combination.2

 

Anatomy & Physiology

The volume of normal adult lungs is about 6 liters, with three lobes making up the right lung and two lobes making up the left. The apices of the lungs may reach 2–3 cm above the medial third of the clavicle, and the bases rest on the diaphragm, which is estimated to be at rib 6 midclavicular, rib 8 midaxillary, and rib 10 posteriorly.3

Visceral pleura covers the lungs while parietal pleura lines the chest cavity. The pleural space is potential space in between the two pleura. Normally, the pleural cavity contains a small amount of fluid to minimize friction. This is a potential space, meaning it has the potential to be filled with air, fluid, or blood—all of which can affect ventilation.4

The pleural membranes may adhere to one another causing pain. EMS providers should be aware of pleurisy or pleuritis, which causes pain during inhalation due to the friction.5

The alveoli are the termini of airflow in the human body. The average human adult has 300 million alveoli, comprising a total surface area of 150 m.6 Gas exchange between inspired air and blood in surrounding capillaries occurs here.

Oxygen concentration is higher in the alveolar space than in the surrounding capillaries, which causes oxygen to diffuse into the blood along a concentration gradient. Carbon dioxide concentration is higher in the capillaries that in the alveolar space. Capillary walls consist of a single layer of cells creating the perfect environment for diffusion of oxygen from the alveolar space to the capillary blood. Conversely, CO2 readily diffuses from capillary blood into the alveolar space.

Pulmonary circulation contains approximately 500 mL of blood, 100 mL of which is available for gas exchange in the capillary bed. Based on Fick’s law, which states that blood flow is proportional to the difference in concentration of a substance in the blood as it enters and leaves an organ, the large surface area of the alveoli and thin membranes of both the alveoli and capillaries allow for efficient gas exchange.7

The act of inspiration is an active process involving the diaphragm and external intercostal muscles. The ribs and sternum move superior as the diaphragm contracts flattening downward. Air rushes into the lungs because the intrapulmonary pressure is less than extra pulmonary pressure, a principle called Boyle’s Law, which states that pressure and volume are inversely proportional for a fixed amount of an ideal gas kept at a fixed temperature. During labored breathing, accessory muscles, such as the scalenes and sternocleidomastoids, assist with raising the ribs to increase space.

This increase in volume due to muscle contraction creates a relative negative pressure space compared to the air pressure outside the body. Boyle’s law states pressure is inversely related to volume, so increasing the volume will decrease the pressure. Creating this concentration gradient between the lungs and the outside environment allows air to be drawn into the lungs; from diffusion, air will move from an area of higher concentration to lower concentration. Ventilation quickly becomes impaired when this gradient is disturbed, such as in tension pneumothorax.

difficulty breathing, air hunger
This patient appears
anxious and hungry for air.

Typically expiration is a passive process in which the muscles relax, reducing the space available in the lungs. This increases intrathoracic pressure above extra thoracic pressure, forcing air out of the lungs. Air is forced out of the lungs when the ribs, sternum, and diaphragm return to their original position. During labored breathing, internal and external muscles actively work to force air out of the lungs.

Increases in intra-abdominal and intra-thoracic pressures assist with venous return to the heart. The increase in pressure squeeze blood in the pulmonary veins and inferior vena cavae to maintain venous return, otherwise known as the respiratory pump.8

 

Pathophysiology

Several terminologies are associated with injuries to the lungs. Pneumothorax is defined as the presence of air in the pleural space. Hemothorax is defined as blood accumulation in the pleural space.4 A tension pneumothorax involves pressure filling the pleural space, which causes ventilation to be impaired and pulmonary circulation to be shunted toward the unaffected lung.

Tension pneumothorax is rapidly lethal because the increasing intrathoracic pressure eventually displaces mediastinal structures, which can interfere with venous return to the heart, causing cardiovascular collapse and shock.

Early signs of tension pneumothorax may include agitation, air hunger, and an increase in respiratory rate. Mental status change and diminished breath sounds on the affected side may be found as the pneumothorax expands. Other signs and symptoms include:

Other less common signs and symptoms include:

The clinical signs are variable, and  a high index of suspicion is needed. The patient will need close and frequent evaluation.

As pressure continues to build in the pleural space, mediastinal shift occurs away from the building pressure. This results in compression of the vena cava and decreased venous return or cardiac preload. The late stage of tension pneumothorax includes such signs as jugular venous distension, tracheal deviation, cyanosis, apnea, and hyperresonance on percussion.

Tachycardia and tachypnea are early compensatory changes as the body attempts to respond to hypoperfusion. Left untreated, tension pneumothorax can quickly cause irreversible shock and death.1

 

Epidemiology

Pneumothorax is a rapidly deteriorating condition that requires early action. Pulmonary conditions commonly associated with tension pneumothorax in one 1978 included pneumonia, pulmonary emphysema, and pulmonary embolism, while procedures most frequently associated with pneumothorax were mechanical ventilation and CPR attempts.9 In cases of penetrating trauma resulting in pneumothorax, 75% will also include hemothorax.10

Although a pneumothorax from any cause can develop into a tension pneumothorax, this condition is most often caused by traumatic injuries. Any injury to the chest can cause rib fractures, which may damage blood vessels and lung tissue. Liman, et al. found an association of hemothorax or pneumothorax development with the presence of rib fractures; 24.9% of patients with one rib fracture and 81.4% of patients with two or more rib fractures also had a hemothorax or pneumothorax.6

From the Vietnam Wound Data and Munitions Effectiveness Team study, researchers found that tension pneumothorax was the cause of death for 3–4% of fatally wounded combat casualties, (e.g., penetrating trauma).11

Although suspicion of tension pneumothorax should remain high for patients with rapidly developing shock, it is rare in primary spontaneous pneumothorax because it is normally associated with traumatic injuries.12

 

Assessment

The primary survey for any patient with difficulty breathing begins with a general observation of the patient’s appearance, and their work of breathing. The patient with tension pneumothorax is no different. An accurate exam requires the chest to be exposed, observed and palpated.13,14

Bare Chest Palpation
Hands on the bare chest accurately
assesses mechanics of breathing
in the field.

Work of breathing will be heavy, the more severe the tension, the less lung tissue is able to expand. Look for such signs of “air hunger” as the use of accessory muscles, and rapid and shallow breaths due to decreased tidal volume. If visible, cyanosis or an ashen color will indicate poor perfusion.

Palpation: EMTs and paramedics work in difficult environments. Palpation of the chest and feeling for un-equal chest rise is a much more reliable and sensitive method of discovering a pneumothorax than simple observation. Rapidly place your hands on both sides of the anterior chest. Each time, ask the patient to take a breath. This will reveal the quickest and some of the most reliable assessment of chest excursion on movement.

Normally the more detailed exam of the chest is left for the secondary survey. In the case of a life threat, such as tension pneumothorax, the suspicion that breathing and circulation is being impaired should prompt you to interrupt a traditional approach, and immediately look for other signs confirming tension pneumothorax. With experience, providers palpating for equal rise should simultaneously be able to note any crepitation or rib instability, cool skin temperature, clammy skin, and the presence of subcutaneous air. All of these findings may suggest a tension pneumothorax and the presence of shock.

Feeling for bilateral radial pulses, rapidly noting character and speed, should reveal tachycardia and weak pulses if tension pneumothorax is present. Change in pulse quality that occurs during inhalation may signal pulsus paradoxus. Pulsus paradoxus is a change in pulse quality, or even the dissapppearance of the pulse due to a fall in left ventricular stroke volume reflected as a fall in systolic blood pressure.Tension pneumothorax is a extracardiac pulmonary cause of pulsus paradoxus.15

A simple pneumothorax by definition will not disrupt circulation. However, because tension pneumothorax decreases cardiac output, the patient will be tachycardic. The heart speeds up to compensate for the decreases in stroke volume.8

pulse check, palpation, pulse strength, pulse rate, pulse equality, pulse check and shock
Feeling for strength, rate and equality
of pulses can help identify
the initial stages of shock.

Late and unreliable signs: Increasing tension may include tracheal deviation (or tracheal “tugging”) and jugular vein distension (JVD).16 Simple visual inspection is unreliable in detecting tracheal deviation. Bates’ guide to physical examination recommends placing your fingers on either side of the trachea to determine if the distance between the trachea and the sternocleidomastoid muscle is equal bilaterally.18 Prehospital Trauma Life Support (PHTLS) indicates the trachea is bound to the cervical spine and fascia, and deviation would be detected lower, at the sternal notch.

In this case, providers would simply feel the deficiency of the trachea if it has shifted to one side.17 These authors also point out that JVD might not be present either. If tension pneumothorax results in decreased cardiac output with hypotension, it is not likely to cause JVD. Note that although tracheal deviation is rare, it is primarily a sign of tension pneumothorax. In contrast, JVD can be present in multiple conditions, such as cardiac tamponade, so it is not necessarily an obvious tension pneumothorax finding.

Diagnostic technologies: The use of ultrasonography in the out-of-hospital environment has been reported.18-22 Paramedics in Texas and Washington have used the technique to better assess and confirm pneumothorax. Researchers have reported training 57 EMT and paramedic students in ultrasound for detection of pleural effusion and pneumothorax. The class was one hour in duration and accuracy of diagnosis was 55–95%.23 The use of ultrasound in the field is still a novel concept, and technology is still developing. As this technology becomes more portable, rugged and affordable EMS systems may find it more realistic to adopt. The future widespread adoption of this technology is still in question.

 

Treatment

Definitive treatment for tension pneumothorax involves decreasing the intrapleural pressure to allow the affected lung to re-expand and blood to return un-impaired to the heart. When the field diagnosis is made, immediate needle decompression should be performed introducing a large-bore catheter (e.g., 14 gauge or larger) into the pleural space at the second intercostal space at the mid-clavicular line. Chest wall thickness may vary. Although an average adult chest should be 4.5 cm thick, researchers have predicted that as many as 35% of the U.S. patient population might has significantly thicker chest walls.24,25 Researchers have also found that as many as 26% of chest decompressions failed because they were possibly too shallow.26

In a 2010 study comparing helicopter and ground EMS crews, researchers found a 65% failure rate when shorter needles were used. They recommend needles that are at least 2 inches (5cm) long.27 Longer needles may be needed. 

If you don’t have a one-way valve, also called a Heimlich valve, try creating a flutter valve. Use the finger of a glove to create a flutter valve by placing the finger over the catheter hub, then cutting a small hole in the end of it.28 There is some disagreement on the benefit of a Heimlich valve. According to the 8th edition of the Prehospital Trauma Life Support (PHTLS), the diameter of the decompression catheter is significantly smaller than the patient's airway, which means it is unlikely that any air movement through the catheter will significantly compromise ventilatory effort. Thus, creation of a Heimlich valve is probably unnecessary form a clinical standpoint.

Immediate improvement should be noted after inserting the needle. Reassessment of vital signs is essential. Use of a one-way valve, such as a flutter valve, may be helpful in improving the mechanics of breathing. This valve will theoretically shut when the patient inhales (e.g., negative pressure in the chest), and allow air to escape the chest (e.g., flutter valve opens) when the patient exhales. No studies exist showing the effectiveness of this valve. Commercially available Heimlich valves are in use in some EMS systems.

Heimlich valve, flutter valve
Create a flutter valve
with the finger of a glove
placed over the catheter hub.

If needle decompression fails to produce improvement, or is not available, basic out-of-hospital care involves assisting ventilations and supplemental oxygen. Providers should note that assisting ventilations may cause the tension to worsen, and should only be performed as a last resort. Failure to get improvement after needle decompression may also indicate that the diagnosis was wrong. A reassessment of the overall diagnosis may also be appropriate.

EMS providers should maintain good situational awareness and not fixate on one problem. If mechanism existed to create a tension pneumothorax, then other traumatic injuries may also be present. Thorough assessment and monitoring of the patient’s condition is also essential. Look for other causes, injuries and co-morbidities.

It is important to reiterate that assessment and definitive field diagnosis can be complicated by noise, movement and varied temperature and light conditions. It is best to keep a high index of suspicion and identify early signs of growing tension (tachycardia, difficulty breathing, diminished lung sounds, pulse quality changes, or unequal chest expansion).29 Hypotension is a late sign which would indicate a higher tension and longer progression of the tension pneumothorax.8

If an object is impaled it should be left in place if possible. Removal may cause greater injury as the object shears tissues and possibly releases pressure that results in additional bleeding.

 

Conclusion

Any injury between the umbilicus and the nipple line should be considered both a possible thoracic injury and a possible abdominal wound. EMS clinicians must maintain a high index of suspicion for tension pneumothorax.

A common error in treating tension pneumothorax is to use a short needle for chest decompression. A large bore (14g or larger) needle with a catheter that is at least 2 inches (5 cm) long is needed to reach the pleural space with reliability in most patients.

 

References

  1. Porth C. Essentials of pathophysiology. 3rd ed. Philadelphia: Wolters Kluwer Health, Lippincott Williams & Wilkins. 2011.
  2. Light RW. Disorders of the pleura, mediastinum, and diaphragm. In: Kasper DL, Braunwald E, Hauser S, Longo D, Jameson LJ, Fauci AS. Harrison’s principles of internal medicine. 16th ed. New York: McGraw-Hill. 2005. p. 1565-69.
  3. Dartmouth Medical Center [Internet]. O’Rahilly; c2008. Swenson R, Caitlin B, Lyons, J. Chapter 22: The pleurae and lungs. Available from: http://www.dartmouth.edu/~humananatomy/part_4/chapter_22.html
  4. Tortora GJ, Derrickson BH. Principles of anatomy & physiology. Hoboken, NJ: Wiley & Sons. 2012.
  5. Anderson K. Mosby’s medical, nursing, & allied health dictionary. St. Louis: Mosby.1998.
  6. Ochs M, Nyengaard JR, Jung A, Knudsen L, Voigt M, Wahlers T, Richter J, Gundersen HJ. The number of alveoli in the human lung. Am J Respir Crit Care Med. 2004 Jan 1;169(1):120-4. Epub 2003 Sep 25.
  7. Wilmore JH, Costill DL, Kenney WL. Physiology of sport and exercise, 4th ed. Champaign, Ill: Human Kinetics. 2008
  8. Leigh-Smith S, Harris T. Tension pneumothorax—time for a re-think? Emerg Med J. Jan 2005; 22(1):8–16. doi: 10.1136/emj.2003.010421
  9. Ludwig J, Kienzle GD. Pneumothorax in a large autopsy population. A study of 77 cases. Am J Clin Pathol. 1978 Jul;70(1):24-6.
  10. Liman ST, Kuzucu A, Tastepe AI, Ulasan GN, Topcu S. Chest injury due to blunt trauma. Eur J Cardiothorac Surg. 2003 Mar;23(3):374-8.PMID 12614809.
  11. McPherson JJ, Feigin DS, Bellamy RF. Prevalence of tension pneumothorax in fatally wounded combat casualties. J Trauma. 2006 Mar;60(3):573-8.
  12. Noppen M. Spontaneous pneumothorax: Epidemiology, pathophysiology and cause. Eur Respir Rev. 2010 Sep;19(117):217-9. doi: 10.1183/09059180.00005310.
  13. American College of Surgeons Committee on Trauma, National Association of EMTs. Prehospital Trauma Life Support (PHTLS). 7th ed. Burlington, Mass: Jones & Bartlett Learning. 2011. p. 114, 301.
  14. Bickley L. Bates' guide to physical examination and history-taking, 11th ed. Philadelphia: Wolters Kluwer Health, Lippincott Williams & Wilkins. 2013. p. 305.
  15. Khasnis A, Lokhandwala Y. Clinical signs in medicine: Pulsus paradoxus. J Postgrad Med. 2002 Jan-Mar;48(1):46-9.
  16. Tintinalli J, Stapczynksi. Ma OJ, Cline D, Cydulka R, Meckler G. Tintinalli's emergency medicine: A comprehensive study guide, seventh edition. 7th ed. New York: McGraw-Hill. 2011. p. 1745.
  17. Di Bartolomeo S, Sanson G, Nardi G, Scian F, Michelutto V, Lattuada L. A population-based study on pneumothorax in severely traumatized patients. J Trauma. 2001 Oct;51(4):677-82.
  18. Bowman J. Visible improvement. JEMS. 2010 Sep;35(9):36-8, 40, 42, passim. doi: 10.1016/S0197-2510(10)70229-1.
  19. Razzaq QM. Use of the ‘sliding lung sign’ in emergency bedside ultrasound. Eur J Emerg Med. 2008 Aug;15(4):238-41. doi: 10.1097/MEJ.0b013e3282f4d15b.
  20. Clinical Trials [Internet]. Bethesda, Md: National Libraries of Medicine. C2014. Bowman JP. Keller Prehospital ultrasound study. Keller Fire Rescue. University of Texas Health Science Center San Antonio. Available from: http://clinicaltrials.gov/show/NCT01074112
  21. Hoyer HX, Vogl S, Schiemann U, Haug A, Stolpe E, Michalski T. Prehospital ultrasound in emergency medicine: Incidence, feasibility, indications and diagnoses. Eur J Emerg Med. 2010 Oct;17(5):254-9. doi: 10.1097/MEJ.0b013e328336ae9e.
  22. Journal of Emergency Medical Services [Internet]. San Diego: Pennwell Corp. c2012. Tinkoff G. Cipolle MD, Rhodes, M. How to recognize & treat the 12 types of thoracic injuries. Available from: http://www.jems.com/deadly-dozen.
  23. Pierog JE, Zaia BE, Bhat SR, Johnson DA, Gharahbaghian L, Gilbert GH, Williams SR. Out-of-hospital evaluation of effusion, pneumothorax and standstill: EMS and point-of-care ultrasonography. Ann Emerg Med. 2010;56;p-S115; Abstract 355:2010. doi: http://dx.doi.org/10.1016/j.annemergmed.2010.06.412
  24. McLean AR., Richards ME, Crandall CS, Marinaro JL. Ultrasound determination of chest wall thickness: Implications for needle thoracotomy. Am J Emerg Med. 2011 Nov;29(9):1173-7. doi: 10.1016/j.ajem.2010.06.030. Epub 2010 Oct 13.
  25. Ullman EA, Donley LP, Brady WJ. Pulmonary trauma emergency department evaluation and management. Emerg Med Clin. North Am. 2003 May;21(2):291-313.
  26. Blaivas M. Inadequate needle thoracostomy rate in the prehospital setting for the presumed pneumothorax: An ultrasound study. J Ultrasound Med. 2010 Sep;29(9):1285-9.
  27. Ball CG1, Wyrzykowski AD, Kirkpatrick AW, Dente CJ, Nicholas JM, Salomone JP, Rozycki GS, Kortbeek JB, Feliciano DV. Thoracic needle decompression for tension pneumothorax: Clinical correlation with catheter length. Can J Surg. 2010 Jun;53(3):184-8.
  28. North Carolina College of Emergency Physicians. Standards Procedure (Skill) Chest Decompression. Available from: www.ncems.org/pdf2012/Proc30-ChestDecompression.pdf.
  29. American Academy of Orthopedic Surgeons, Caroline NL, Elling B, Smith M. Nancy Caroline’s emergency care in the streets 7th ed. Burlington, Ma: Jones & Bartlett Publishers; 2012. 730-864.

 

The EMS Reference is a community project, and we encourage your suggestions. Give us your feedback.

Published: January 8, 2015
Revised: November 27, 2015